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首页> 美国卫生研究院文献>Infection and Immunity >Trichomonas vaginalis-Induced Epithelial Monolayer Disruption and Human Immunodeficiency Virus Type 1 (HIV-1) Replication: Implications for the Sexual Transmission of HIV-1
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Trichomonas vaginalis-Induced Epithelial Monolayer Disruption and Human Immunodeficiency Virus Type 1 (HIV-1) Replication: Implications for the Sexual Transmission of HIV-1

机译：阴道毛滴虫诱导的上皮单层破坏和人类免疫缺陷病毒1型（HIV-1）复制：对HIV-1的性传播的影响。

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The objective of this study was to evaluate potential mechanisms of Trichomonas vaginalis involvement in human immunodeficiency virus type 1 (HIV-1) transmission. Polarized monolayer integrity of primary cervical and prostate epithelial cells or cell lines cultured with T. vaginalis was measured by monitoring transepithelium resistance. The effect of T. vaginalis isolates on HIV-1 passage through polarized epithelial cell monolayers was evaluated for HIV-1 p24gag in the basolateral supernatants. Coincubation with T. vaginalis isolates induced disruption of monolayer integrity and resulted in passage of virus to the basolateral side of the monolayer. Furthermore, there was isolate variability in which two isolates induced greater monolayer damage and increased HIV-1 passage than did the other two isolates. Coincubation of T. vaginalis isolates with acutely HIV-1-infected peripheral blood mononuclear cells enhanced HIV-1 replication. This enhancement was associated with cellular proliferation and activation, as well as with tumor necrosis factor alpha production. In contrast to the monolayer disruption, the effect of T. vaginalis on HIV-1 replication was not isolate dependent. Thus, two mechanisms have been identified that could contribute to the epidemiologic association of trichomoniasis with the sexual transmission of HIV-1. (i) T. vaginalis disruption of urogenital epithelial monolayers could facilitate passage of HIV-1 to underlying layers. (ii) Activation of local immune cells by T. vaginalis in the presence of infectious HIV-1 might lead to increased viral replication. Collectively, these data suggest the need for more vigilant efforts in the diagnosis and treatment of T. vaginalis in women and men, especially in countries with a high prevalence of HIV-1.
机译：这项研究的目的是评估阴道毛滴虫参与人类免疫缺陷病毒1型（HIV-1）传播的潜在机制。通过监测跨上皮的抵抗力来测量原代宫颈和前列腺上皮细胞或经阴道锥虫培养的细胞系的极化单层完整性。对于基底外侧上清液中的HIV-1 p24 gag ，评估了阴道分枝杆菌对HIV-1通过极化的上皮细胞单层通过的影响。与阴道锥虫共孵育分离株诱导单层完整性破坏，并导致病毒传到单层基底外侧。此外，存在分离株变异性，其中两个分离株比其他两个分离株诱导更大的单层破坏和增加的HIV-1传递。阴道分枝杆菌与急性感染HIV-1的外周血单核细胞共孵育增强了HIV-1的复制。这种增强与细胞增殖和活化以及肿瘤坏死因子α的产生有关。与单层破坏相反，阴道锥虫对HIV-1复制的作用不是孤立的。因此，已经确定了两种机制，可以促进滴虫病与HIV-1的性传播的流行病学联系。 （i）泌尿生殖道上皮单层的阴道T.破坏可以促进HIV-1传递到下层。 （ii）在感染性HIV-1存在下，阴道锥虫对局部免疫细胞的激活可能导致病毒复制增加。总体而言，这些数据表明，在男性和女性中，尤其是在HIV-1患病率较高的国家中，在诊断和治疗阴道锥虫时需要更加警惕。

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